Non-cardiac chest pain: a 2018 update.

Non-cardiac chest pain (NCCP) is defined as recurring, angina-like, chest pain of non-cardiac origin. Studies have estimated that gastroesophageal reflux disease (GERD) is the most common contributing factor for NCCP. In patients with non-GERD related NCCP, esophageal motility disorders, and functional chest pain of presumed esophageal origin are the main underlying mechanisms for symptoms. Epidemiologic studies show a high prevalence of panic disorder, anxiety and major depression in NCCP patients. The diagnostic esophageal workup starts only after that cardiac and pulmonary diseases have been ruled out. NCCP patients with typical reflux symptoms are more likely to have GERD-related NCCP than those without typical reflux symptoms. High-dose proton pump inhibitor trial (PPI test) can be used to confirm the diagnosis of GERD-related NCCP. Negative upper endoscopy is quite common. For patients unresponsive to antireflux treatment and with negative endoscopy, impedance-pH monitoring should be done. Treatment of patients with non-GERD-related NCCP has focused on esophageal (hypercontractile or spastic) motility disorders and esophageal visceral hypersensitivity. In the first case, several trials using calcium channel blockers, nitrates, anticholinergics, or botulinum toxin injection and recent trials with endoscopic myotomy have been conducted. In case of visceral hypersensitivity, studies found that the amelioration, when compared to placebo, was significant with venlafaxine, sertraline, and imipramine. In this context, also cognitive behavioral therapy has been proposed.

The complexity of globus: a multidisciplinary perspective.

Globus is a topic of interest for many specialties including otorhinolaryngology, gastroenterology and psychiatry/psychosomatic medicine, but, although many hypotheses have been suggested, key questions about its aetiology remain. This Review provides an overview of the extensive literature concerning this topic and discusses the quality of the evidence to date. Globus has been associated with oropharyngeal structural lesions, upper oesophageal sphincter disorders, oesophageal disorders, GERD, psychosocial factors and psychiatric comorbidity. However, findings are often contradictory and the literature remains highly inconclusive. Indeed, with the exception of patients with structural-based globus, the Rome III criteria for functional globus only apply to a subgroup of patients with idiopathic globus. In clinical reality, there exists a group of patients who present with idiopathic (nonstructural) globus, but nevertheless have dysphagia, odynophagia or GERD-exclusion criteria for globus diagnosis according to Rome III. The symptomatology of patients with globus might be broader than previously thought. It is therefore crucial to approach globus not from one single perspective, but from a multifactorial point of view, with focus on the coexistence and/or interactions of different mechanisms in globus pathogenesis. This approach could be translated to clinical practice by adopting a multidisciplinary method to patients presenting with globus.

Systematic review: the treatment of noncardiac chest pain.

BACKGROUND: Treatment of noncardiac chest pain (NCCP) remains a challenge. This is in part due to the heterogeneous nature of this disorder. Several conditions are associated with NCCP including gastro-oesophageal reflux disease (GERD), oesophageal dysmotility, oesophageal hypersensitivity as well as others. AIM: To determine the currently available therapeutic modalities for NCCP. METHODS: We performed a systematic review of the literature that was published between January, 1980 and March, 2011. We identified 734 studies; 68 of them met entry criteria. RESULTS: Patients with GERD-related NCCP should receive proton pump inhibitors (PPI) twice daily for at least 8 weeks. Smooth muscle relaxants are only recommended for temporary relief of NCCP with motility disorders. Botulinum toxin injection of the distal oesophagus may be effective in the treatment of NCCP and spastic oesophageal motility disorders. Studies assessing the value of tricyclic antidepressants, trazodone and selective serotonin reuptake inhibitors in NCCP are relatively small, but suggest an oesophageal analgesic effect in NCCP patients that is limited by their side effects profile. The usage of theophylline to treat patients with non-GERD-related NCCP should be weighed against its potential toxicity. Use of complementary medicine has been scarcely studied in NCCP. Patients with coexisting psychological morbidity or those not responding to any medical therapy should be considered for psychological intervention. Cognitive behavioural therapy and hypnotherapy may be useful in the treatment of NCCP. CONCLUSIONS: Patients with GERD-related noncardiac chest pain should be treated with at least double dose PPI. The primary treatment for non-GERD-related noncardiac chest pain, regardless if oesophageal dysmotility is present, is pain modulators.

[Psychosomatic medicine for non-cardiac chest pain].

Recently, it has become problematic that the number of noncardiac chest pain (NCCP) patients are increasing among those who come to the emergency room with chest pain as a chief complaint. They tend to come to hospitals often and over many years, even after cardiac-chest pain has been excluded from their diagnosis. Moreover, studies have shown that NCCP patients have a high prevalence of anxiety, depression and disability. However, most NCCP patients are usually treated by cardiologists or primary physicians. Ordinary biomedical approaches often fail to treat NCCP. NCCP is one of the most important functional somatic syndromes from the view of medical economics. The cause of NCCP includes gastroesophageal reflux disease, panic disorder and esophageal dysmotility. In this review article, we summarize the definition, epidemiology, pathology, and process of diagnosis of NCCP. Finally, we propose a pathological hypothesis from a psychosomatic view. We discuss the effects of anxiety, fear and hyperactive behavior induced by affective stressors on the dysmotility and the lowering of the pain threshold.

Úlceras acrales y fenómeno de Raynaud en un adolescente / Digital ulcerations and Raynaud´s phenomenon in an adolescent

El síndrome de Crest es una variedad de esclerodermia sistémica; concretamente, una forma limitada. Se considera una forma incompleta de la enfermedad, que presenta un curso más benigno, dado que las afectaciones renal y pulmonar no son sus principales características. Los síntomas fundamentales del síndrome de Crest, que conforman su acrónimo,son: calcinosis, fenómeno de Raynaud, dismotilidad esofágica, esclerodactilia y telangiectasias. Presentamos un caso cuyo inicio se produjo durante la adolescencia, hecho muy poco frecuente, que, sin embargo, presenta un mejor pronóstico que en la edad adulta

Crest síndrome is a type of limited systemic scleroderma. It is considered to be an incomplete form of the disease that has a more benign course, as renal and pulmonary involvement are not is principal characteristics. The major symptoms of Crest syndrome, the initials of which give it its name, are calcinosis, Raynaud´s phenomenon, esophageal dysmotility, sclerodactyly and telangiectasia. We report a case with onset during adolescence, a very uncommon circumstance which however, is associated with a better prognosis than that involving adult onset

High-dose ibuprofen therapy associated with esophageal ulceration after pneumonectomy in a patient with cystic fibrosis: a case report.

BACKGROUND: Lung disease in patients with cystic fibrosis is thought to develop as a result of airway inflammation, infection, and obstruction. Pulmonary therapies for cystic fibrosis that reduce airway inflammation include corticosteroids, rhDNase, antibiotics, and high-dose ibuprofen. Despite evidence that high-dose ibuprofen slows the progression of lung disease in patients with cystic fibrosis, many clinicians have chosen not to use this therapy because of concerns regarding potential side effects, especially gastrointestinal bleeding. However, studies have shown a low incidence of gastrointestinal ulceration and bleeding in patients with cystic fibrosis who have been treated with high-dose ibuprofen. CASE PRESENTATION: The described case illustrates a life-threatening upper gastrointestinal bleed that may have resulted from high-dose ibuprofen therapy in a patient with CF who had undergone a pneumonectomy. Mediastinal shift post-pneumonectomy distorted the patient's esophageal anatomy and may have caused decreased esophageal motility, which led to prolonged contact of the ibuprofen with the esophagus. The concentrated effect of the ibuprofen, as well as its systemic effects, probably contributed to the occurrence of the bleed in this patient. CONCLUSIONS: This report demonstrates that gastrointestinal tract anatomical abnormalities or dysmotility may be contraindications for therapy with high-dose ibuprofen in patients with cystic fibrosis.

Acute and long-term effects of nifedipine on pulmonary and systemic hemodynamics in patients with pulmonary hypertension associated with diffuse systemic sclerosis, the CREST syndrome and mixed connective tissue disease.

Ten patients with pulmonary hypertension associated with diffuse systemic sclerosis (1 patient), the CREST syndrome (calcinosis cutis, Reynaud's phenomenon, esophageal dysmotility, sclerodactyl, telangiectasia) (6 patients) and mixed connective tissue disease (3 patients) were studied to assess the effect of oral nifedipine on pulmonary and systemic hemodynamics. Each patient underwent right-sided cardiac catheterization just before nifedipine administration. Thereafter, oral nifedipine was administered in 10 mg increments every 90 minutes until pulmonary vascular resistance normalized or a total dose of 30 mg was achieved. Hemodynamic measurements were obtained at 30-minute intervals for 3 hours, then hourly for 9 hours (acute study). Hemodynamic studies were repeated 3 to 6 months after the initial catheterization with the minimum dose of oral nifedipine (administered every 8 hours) required to achieve maximal reduction of pulmonary vascular resistance in the acute study (long-term study). In the acute study, oral nifedipine produced a significant decrease in mean pulmonary vascular resistance from 6.3 +/- 3.8 to 4.3 +/- 3.6 U (p less than 0.001). Similar changes in pulmonary vascular resistance were noted in the long-term study (n = 6). The results indicate that oral nifedipine is capable of producing an acute and sustained reduction in pulmonary vascular resistance in patients with pulmonary hypertension associated with diffuse systemic sclerosis, the CREST syndrome and mixed connective tissue disease.